Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
78 Cards in this Set
- Front
- Back
|
what are the 4 columns of general anesthesia?
|
analgesia
amnesia hypnosis immobility |
|
|
what are the 4 stages of general anesthesia?
|
stage I -analgesia
stage 2- excitement stage 3- surgical anesthesia stage 4- medullary depression |
|
|
what occurs in stage 1 gen. anesth.
|
i. Patients experience analgesia without amnesia first; later in stage I, both analgesia and amnesia are produced.
|
|
|
what occurs in stage 2 gen anesth
|
i. Patients appear to be delirious. They may vocalize thoughts, but they are definitely amnesic (won’t remember what they say).
ii. Respiration is irregular in volume and in rate. Laryngospasm may occur. iii. Retching and vomiting may occur if the patient is stimulated. iv. For these reasons, there is an effort to limit the duration and severity of this stage of anesthetic induction. The stage ends when regular breathing is reestablished. |
|
|
when does stage 3 gen anesth occurs
|
i. Begins with the reestablishment of regular respiration and extends to complete cessation of spontaneous respiration (apnea).
|
|
|
what occurs in stage 3 gen anesth
|
ii. Apnea, analgesia, hemodynamic depression.
|
|
|
what occurs in stage 4 gen anesth?
|
e. Stage IV – medullary depression
i. Deep stage of anesthesia that includes severe depression of the vasomotor and respiratory center death may rapidly ensue without support. |
|
|
what is important about doseing for gen. anesth. induction
|
f. For anesthetic induction, you need a large dose to overcome the excitement stage. Later you need a much smaller dose to maintain full anesthesia due to anesthetic equilibrium.
|
|
|
3. Explain the properties of an “ideal anesthetic.”
|
a. Loss of consciousness smoothly and rapidly.
b. Prompt recovery of cognitive function after its administration is discontinued. c. Wide margin of safety and be devoid of adverse effects. |
|
|
what is a factor in potency of volatile(gas) anesthetics but no longer is considered the only factor?
|
potency of anesthetics increases with the lipid solubility. Previously, this was used to describe the mechanism of volatile anesthetics. However, it is no longer accepted as a complete description of the factors that contribute to the potency of an anesthetic.
|
|
|
what is the action of inhaled anesthetics?
|
b. Currently it is thought that the ultimate action of inhaled anesthetics is on specific neuronal membrane proteins that permit the translocation of ions during membrane excitation.
BUT there is large heterogeneity of targets of anesthetics, and that activation/inhibition of one target alone is not sufficient to explain the mechanism of action of anesthetics. |
|
|
what is the process that occurs following GABA receptor binding?
|
iii. Binding of GABA causes a conformational change in the receptor that opens a central pore and allows chloride ions to pass down their electrochemical gradient. *GABA binding causes receptor to open.*
iv. Opening of the receptor and the influx of chloride ions results in a net inhibitory effect, reducing the activity of the neuron. |
|
|
what is minimum alveolar conc.(MAC)
|
d. Minimum Alveolar Concentration
i. Basic unit used to describe anesthetic potency. ii. Is defined as the alveolar concentration of an agent at 1 atm that produces immobility in 50% of subjects exposed to a noxious stimulus (i.e. a scalpel cut). |
|
|
what does MAC decrease with?
|
iii. MAC is decreased with:
1. Co-administration of nitrous oxide 2. Premedication (i.e. with morphine) 3. Increasing age 4. Alcohol intoxication 5. Hypothermia 6. Hypotension 7. Hypercarbia 8. Sympathetic decrease (i.e. administration of clonidine, reserpine, methyldopa) |
|
|
what does MAC increase with?
|
iv. MAC is increased with:
1. Younger age (highest at 6 months) 2. Chronic alcohol abuse due to increased enzyme activity 3. Sympathetic increase (CNS drugs, ephedrine, amphetamines, cocaine, etc) |
|
|
what is the different affects of using higher vs lower levels of anesthesia?
|
v. Cognitive function is decreased at lower levels of anesthesia, mobility is impaired at higher levels. Therefore, you need different levels of anesthesia based on the procedure the patient is undergoing. For example, intubation needs much higher levels than a skin incision.
|
|
|
what are the 3 factors that determine the uptake and distribution of volatile anesthetics?
|
Solubilty of gas, cardiac output (Q) and alveolar-to-venous partial pressure difference (PA-PV).
|
|
|
what is the equation for volatile anesthetic uptake?
|
uptake=solubility *cardiac output*alveolar to venous partial pressure difference
|
|
|
what is another name for solubility?
|
blood/gas partition coefficient
|
|
|
what is the correlation btw uptake of volatile anesthesia and speed of action?
|
e. Greater solubility and greater uptake actually mean that there will be a slower onset of anesthetic action. A lot of agent is disappearing into the body, but blood levels rise slowly and the patient takes a long time to go to sleep. Recovery is also slower with more blood soluble agents.
|
|
|
what is important about the Brain/blood partition coefficient?
|
All anesthetics have a fairly high brain/blood partition coefficient. Drugs with low blood solubility reach sufficient brain levels more quickly.
|
|
|
explain in ur own words the various partition coefficients and their effect on anesthetics
|
alveolar/blood- if there is high solubility in blood then it will absorb quickly from the alveoli but then it wont diffuse out of the blood quickly to the target tissue
blood/brain-all anesthetics prefer to dissolve in tissue, espeacially fat and brain blood/muscle- anesthetics pass quickly into muscle, not sure if this is good or bad yet blood/fat- anesthetics pass quickly into fat just like brain but fat has little blood supply and brain has a massive blood supply so this isnt a big deal |
|
|
what is the problem with Halothane, Isoflurane, and Enflurane.
|
a. Older inhaled anesthetics include Halothane, Isoflurane, and Enflurane. These drugs have higher blood solubility and therefore a slower onset of action. These drugs are also more extensively metabolized, especially halothane. Halothane undergoes 40% metabolism.
|
|
|
what is useful about the new anesthetics?
|
b. Newer inhaled anesthetics include Desflurane and Sevoflurane. These drugs are less blood soluble and therefore have a much quicker onset of action. They also undergo very limited metabolism. Metabolism can decrease the amount delivered to the brain/make it less predictable, so low metabolism is desirable.
|
|
|
what are the newer inhaled anesthetics?
|
b. Newer inhaled anesthetics include Desflurane and Sevoflurane
|
|
|
9. Describe the “second gas effect” and how it affects onset and recovery of inhalational anesthesia. (summarize this one is long)
|
a. The second gas effect refers to the administration of a drug along with nitrous oxide and oxygen. Nitrous oxide has low solubility, but it is administered at very high concentrations so there is still significant uptake from the alveoli. The gas mixture administered contains a large amount of nitrous oxide and a small amount of the second gas. A certain amount of the nitrous oxide is taken up (50% in the example) which leads to an increased concentration of the second gas in the alveoli due to the decreased total volume. Subsequent ventilation replaces the lost volume with the same proportions of nitrous oxide, oxygen, and second gas, further increasing the concentration of second gas in the alveoli.
b. The result of this is a quicker onset of anesthesia. c. Increased ventilation will also result in a quicker onset of anesthesia. |
|
|
a. The half-life of the IV anesthetics is “context-sensitive.” This means
|
that the duration of action, or time to recovery, will increase with increased duration of infusion.
|
|
|
what three IV anesthetics have shorter half lifes than the others?
|
Etomidate, propofol, and ketamine have significantly shorter half-times , which makes them more suitable for prolonged infusion.
|
|
|
which IV anesthetics have longer half lifes?
|
thiopental and diazepam
|
|
|
which IV anesthetics is prefered for prolonged infusion
|
Etomidate, propofol, and ketamine have significantly shorter half-times , which makes them more suitable for prolonged infusion.
|
|
|
what are the barbiturates used most often in IV anesthetics
|
i. Thiopental
|
|
|
what is the metabolism of barburates?
|
ii. With the exception of phenobarbital, all barbiturates are hepatically metabolized and excreted in the urine.
|
|
|
what determines the duration of action of barbiturates in IV anesthesia?
|
iii. Duration of action is determined by re-distribution of drug within and between different physiological compartments, rather than metabolism.
|
|
|
elimination of propofol?
|
i. Rapidly metabolized in the liver by conjugation to glucuronide and sulfate to produce water-soluble compounds which are excreted by the kidney. Propofol’s clearance exceeds hepatic blood flow, which suggests extrahepatic metabolism as well. This most likely occurs in the lung.
|
|
|
what is the duration of action for propofol?
|
ii. Has a short context-sensitive half-time because of its extremely high clearance (extensive metabolism)
|
|
|
what make the termination of action for etomidate?
|
i. Termination of action occurs by redistribution.
|
|
|
ketamine metabolism?
|
i. Extensively metabolized by hepatic microsomal enzymes.
|
|
|
what is the benzo used in IV anesthesia?
|
midazolam
|
|
|
what is the standard induction agent in IV anesthesia?
|
thiopental
|
|
|
which drug is used to balance anesthesia and conscious sedation?
|
midazolam
|
|
|
which anesthesia is standard induction for CHF patients?
|
etomidate
|
|
|
what is the reversal agent to midazolam?
|
flumazenil
|
|
|
when is thiopental expcitely contraindicated?
|
in porphyrias
|
|
|
where is consiousness controled in the brain?
|
cerebral cotex, thalamus, and reticular formation
|
|
|
what receptors are in high concentrations in the areas of brain that control consciousness?
|
y-aminobutyric acid(GABA), n-methyl-d-asparate (NMDA) and acetylcholine(Ach)
|
|
|
where is immobility controlled and with what main receptor?
|
sensory and motor neurons
GABAa receptors,main one also present inhibitory glycine receptor inhibit post syntaptic AMPA and NMDA sensitive glutamate receptors |
|
|
where is analgesia located? with what recepotors?
|
spinal cord
glutamate, GABAa, receptors. |
|
|
where is amnesia controled
|
hippocampus, amygdaly and prefrontal cortex
|
|
|
what is inhibited to cause amnesia?
|
neuronal nicotinic acetylcholine receptors
|
|
|
what other physiologic effects occur in anesthisia other than what we want
|
hemodynamic
respiratory hypothermia nausea/vomiting |
|
|
define MAC
|
minimal anesthetic concentration
minimum alveolar concentration at 1atm of an agent that produces immobility in 50% of people. |
|
|
what happens to MAC with addition of NO2?
|
decrease its effective MAC(which means you need less to get what you want)
|
|
|
what are the most important MAC modulators?
|
AGE
and Nitrous oxide |
|
|
what is the MAC of Amnesia/unconsiousnes/and immobility in relation to each other?
|
MAC is lowest for amnesia
MAC is WAY higher for immorbiilty MAC is a little higher than amnesia and significantly lower than immobility |
|
|
what is the ideal desire for qualities of volatile anesthetics?
|
low blood/gas partition
high brain/blood partition low metabolism low MAC |
|
|
what happens to Uptake with increase in ventalation?
|
increases uptake
|
|
|
what happens to alveolar concentration with increased cardiac output?
|
decreases alveolar concentration
|
|
|
what is cardiovascular effect of the volatile anesthetics?
|
all of them depress cardiovascular function
halothane and enflurane act as direct cardio-depressants sevoflurane, desflurane, and isoflurane cause a reduction in system vascular resistance Halothane reduces HR, while desfluran adn isoflurane increase HR volatile anesthetics reduce myocardial oxgen consumption and act against myocardial reperfusion injury isoflurane can cause a coronary steal phenomenon |
|
|
what is a problem with isoflurane in cardiac problem patients?
|
isoflurane can cause a coronary steal phenomenon which means it dilates healthy vessels but doesnt dilate unhealthly ones this leads to even less blood getting to the ischemic areas of the heart
|
|
|
what are the respiratory effects of volatile anesthetics
|
decreased tidal volume and increased rate
increased apneic threshold depress mucocilliary function in the airway |
|
|
what is apneic threshold?
|
CO2 level below which apnea occurs through lack of CO2 driven respiratory stimulation ie decreases the ventilaorty response to hypoxia
|
|
|
what are the implications of depressed mucocilliary function in the airway?
|
risk of atelectasis(collapse) and postoverative resp. infections.
|
|
|
what are the effects of volatile anasthesia on kidney and liver?
|
MAY reduce blood flow
may reduce autoreg of kidney |
|
|
what is a the only drug with both anesthic and analgesic properties?
|
nitrous oxide
|
|
|
halothan hepatitis?
|
halothan is metabolized to a reactive metabolite TFA-CL which is further changed to TFAA which binds to liver hepatocytes and causes hepatitis
halothan not used much in US |
|
|
what is Florid-induced nephrotoxity?
|
sevoflurane when metabolized releases floride ion which can damage the kidney if used for long duration
|
|
|
what is the main known anethesiac emergency?
|
malignant hyperthermia
|
|
|
what are the signs of malignant hyperthermia?
|
first signs
-hypercabia(highCO2) -sinus tachycardia -masseter spasm drop to really high temp 40 decrees C respiratory acidosis and muscular abnormalities |
|
|
which volatile anesthetics can cause malignant hyperthermia?
|
all of them
|
|
|
what is the MOA of malignant hyperthermia?
|
dihydropyridine recpetor couples the ryanodine receptor on the transverse tubules in the sarcoplasmic reticulum of myocytes. the job of these receptors is to allow Ca to flow into the myoplasm and cause contraction
in some people there is a raynodine receptor(RyR) mutation that leads to 3 times normal Ca release when binding the anesthetics. this causes tetany and increased SKM metabolism and heat production. |
|
|
what is the chromosome associatied with the mutation that causes malignant hyperthermia?
|
chromosome 19
|
|
|
what should be done to treat malignant hyperthermia?
|
discontinue triggering agent and start 100% O2 high flow, give dantoliene to titrate the effect
|
|
|
when is ketamine advantagous to use?
|
when patient is in hypovolumeic shock this is only one that doesnt lower BP
|
|
|
what is the MOA of barbiturate redistribution?
|
brain absorbes the drug much faster than the other tissues but there is so much more tissue of fat and lean muscle that as the blood level drops the drug is leached from the brain back into the blood and depostied in the fat.
|
|
|
which drug has a dissociative anesthesia?
|
ketamine
means they dont stop breathing good for patients in ER that you are worried about airway. |
|
|
what is the to types of ketamine?
|
ketamine S and R
US only uses R form but S for is stronger with more side effects |
|
|
which drugs does not affect GABAa ?
|
ketamine
|
|
|
what is the drug target of ketamine?
|
acts on NMDA recptors, opoid receptors, monoaminergic receptros, muscarine receptros and voltage sensitive calcium channels
|
